Evaluation of chemerin and its receptors, ChemR23 and CCRL2, in gingival tissues with healthy and periodontitis

Abstract

Chemerin is a chemoattractant protein that directs inflammatory cells that express its receptor chemokine receptor-like 1 (ChemR23) towards sites of inflammation. C-C chemokine receptor-like 2 (CCRL2), is the other receptor of chemerin, improves the interaction between chemerin and ChemR23. The aim of this study was to evaluate the expression of chemerin and its receptors in gingival tissues with healthy and periodontitis. Tissue biopsy samples were obtained from 20 patients with chronic periodontitis and from the gingiva of 20 healthy individuals undergoing a crown lengthening process. Quantitative real-time PCR (qPCR) was used to examine the mRNA expression of chemerin, ChemR23 and CCRL2. Additionally, protein expression was measured by immunohistochemistry. Both qPCR and immunohistochemistry results revealed that the expression of chemerin and ChemR23 was significantly higher in tissues with periodontitis than in healthy tissues (P = 0.001 and, P = 0.015, respectively). There were no significant differences between healthy tissues and those with periodontitis in terms of mRNA expression of CCRL2, whereas a more intense staining was observed in tissues with periodontitis. The mRNA expression levels of chemerin showed a positive correlation with plaque index, gingival index, probing pocket depth and clinical attachment level (r = 0.448, r = 0.460, r = 0.439 and, r = 0.459, respectively, P< 0.01). To the best of our knowledge, this study is the first to examine the expression of chemerin, ChemR23 and CCRL2 in gingival tissues. Our study suggests that chemerin may play a role in the pathogenesis of periodontitis by causing chemoattraction of immune cells that direct ChemR23 receptors to the site of inflammation.

Adipokines and Inflammation: Focus on Cardiovascular Diseases

“…Chemerin was first identified as a novel retinoid-responsive gene in psoriatic skin lesions [ 80 ]. In addition to skin, chemerin is widely expressed throughout the human body and is mainly produced by the liver, WAT, and placenta [ 70 ] but is also found in the brain, spinal cord, spleen, lymph node, thymus, stomach, small intestine, colon, kidneys, testis, ovary, pituitary, lungs, heart, skeletal muscle, pancreas, arteries, cartilage, or gingival tissues [ 74 , 81 , 82 , 83 , 84 , 85 , 86 ]. The adipose tissue production of chemerin and CMKLR1 receptor in humans and mice was described in 2007, when chemerin came to be considered a new adipokine [ 87 ].…”

A genome-wide association analysis: m6A-SNP related to the onset of oral ulcers

“…Oral ulcers are characterized by the inflammatory reactions of mucosal epithelial tissues in the oral cavity. During this process, chemokines, chemokine receptors and immune cells will all increase significantly ( 50 , 51 ). Therefore, the abnormal expression of the gene CCRL2 in mucosal tissues is very likely to trigger inflammation and then induce the occurrence of oral ulcers, and m6A-SNPs play an important role in this process.…”

Chemerin/ChemR23 regulates cementoblast function and tooth resorption in mice via inflammatory factors

“…Chemerin is also believed to be associated with a variety of chronic inflammatory conditions. Furthermore, some researchers have reported that chemerin and its receptors ChemR23 are expressed in periodontal tissues 18,35–37 . To elucidate the mechanism of action of chemerin, we knocked down ChemR23 in cementoblasts.…”

“…Furthermore, some researchers have reported that chemerin and its receptors ChemR23 are expressed in periodontal tissues. 18,[35][36][37] To elucidate the mechanism of action of chemerin, we knocked down ChemR23 in cementoblasts. Unlike virus-mediated methods, transfection approaches using LipoHigh cannot induce permanently stable gene silencing; however, we were able to verify the changes in protein expression via Western blot analysis.…”